Quadruple therapy as first choice for eradication of H. pylori due to clarithromycin-resistance

Helicobacter pylori is associated with benign and malignant diseases of the upper gastrointestinal tract. Increasing antibiotic resistance has made alternative treatments necessary.

Diagnosis of Helicobacter pylori infection: 13C urea breath test or the stool antigen test as “test and treat strategy”. BMJ, 2012.

Empirical triple therapy (proton-pump inhibitor, clarithromycin, amoxicillin) is currently the first choice for eradication of Helicobacter pylori. As antibiotic resistance to clarithromycin (which has a crucial role in eradication) has increased. The eradication rate with triple therapy has gradually decreased below 80%, and even less.

The aim of this study reported in The Lancet was to assess the efficacy and safety of a new, single-capsule treatment versus the gold standard for H. pylori eradication (triple therapy).

A randomised, open-label trial of adults with H. pylori infection compared the efficacy and safety of:

- quadruple therapy: 10 days of quadruple therapy with omeprazole plus a single three-in-one capsule containing bismuth, metronidazole, and tetracycline

- standard therapy: 7 days of omeprazole, amoxicillin, and clarithromycin (editor note: why not 14 days of therapy?)

H. pylori eradication was established by negative 13C urea breath tests at 28 and 56 days after the end of treatment.

The eradication rates were 80% in the quadruple therapy group versus 55% in the standard therapy group.

The study authors concluded that quadruple therapy should be considered for first-line treatment in view of the rising prevalence of clarithromycin-resistant H. pylori. Quadruple therapy provides superior eradication with similar safety and tolerability to standard therapy.

References:

Helicobacter pylori eradication with a capsule containing bismuth subcitrate potassium, metronidazole, and tetracycline given with omeprazole versus clarithromycin-based triple therapy: a randomised, open-label, non-inferiority, phase 3 trial. The Lancet, Volume 377, Issue 9769, Pages 905 - 913, 12 March 2011.

Quadruple or triple therapy to eradicate H pylori. The Lancet, Volume 377, Issue 9769, Pages 877 - 878, 12 March 2011.

H. pylori eradication provides benefits to patients with functional dyspepsia http://goo.gl/UwxsT

H. pylori image courtesy of www.hpylori.com.au.

Celiprolol as treatment of choice to prevent complications in vascular Ehlers-Danlos syndrome

Vascular Ehlers-Danlos syndrome is a rare hereditary connective tissue disorder caused by mutations in the collagen type III gene ( COL3A1 ), which leads to a loss of tissue integrity in many organ systems.

Patients with vascular Ehlers-Danlos syndrome have weakened blood vessels and an increased risk of arterial dissection or rupture that can lead to early death.

The researchers assessed the ability of celiprolol, a β1-adrenoceptor antagonist with a β2-adrenoceptor agonist action, to prevent arterial dissections and ruptures in vascular Ehlers-Danlos syndrome.

Patients with clinical vascular Ehlers-Danlos syndrome were randomly assigned to 5 years of treatment with celiprolol or to no treatment.

33 patients were positive for mutation of collagen 3A1 (COL3A1). Celiprolol was uptitrated every 6 months by steps of 100 mg to a maximum of 400 mg twice daily. The primary endpoints were arterial events (rupture or dissection, fatal or not).

Mean duration of follow-up was 47 months, with the trial stopped early for treatment benefit.

The primary endpoints were reached by 20% in the celiprolol group and by 50% controls (hazard ratio [HR] 0·36).

Celiprolol might be the treatment of choice for physicians aiming to prevent major complications in patients with vascular Ehlers-Danlos syndrome.

References:

Effect of celiprolol on prevention of cardiovascular events in vascular Ehlers-Danlos syndrome: a prospective randomised, open, blinded-endpoints trial. The Lancet, Volume 376, Issue 9751, Pages 1476 - 1484, 30 October 2010.

Celiprolol therapy for vascular Ehlers-Danlos syndrome. The Lancet, Volume 376, Issue 9751, Pages 1443 - 1444, 30 October 2010.